If you’ve followed any of the discussion about high fructose corn syrup (HFCS) vs. sucrose, you’ve probably heard representatives of the soft drink industry and HFCS refiners repeatedly say that fructose is no different than sucrose and that they’re metabolized the same (which, according to more and more research, is debatable). I’ll get to that a little further on.

How much sugar we’re consuming

Make note of that 31.1 teaspoons per day figure for 2001. (Daily intake in teaspoons = average annual intake in pounds / 365 days per year x 16 ounces per pound x 28.3495 grams per ounce / 4.2 grams per teaspoon.)

Think about the last item in that formula. If the label on a box of cereal says 9 g of sugars, that means that a single serving contains 2 tsps of sugar. A 12 oz. soda containing 39 g of sugars contains more than NINE teaspoons of sugar. You get the idea.

According to Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005 (see references), for 2005 it was down to 30 teaspoons per day.

What does this tell us?

Several points, one, representatives of the Corn Refiners Association and beverage manufacturers are right when they say that whether it’s fructose or sucrose doesn’t really matter. If you’re consuming almost 4 times the amount of added sugars you should be, you are going to have problems!

Two, sucrose contained in beverages begins to undergo hydrolysis once it’s bottled and separates into its component parts (that is, fructose and glucose). So in many cases when you’re drinking a sugar-sweetened soda you’re not drinking sucrose in solution, but sucrose, fructose, and glucose. If enough time goes by most of the sucrose turns into free fructose and glucose.

A number of studies have shown that fructose is metabolized differently than glucose, but other studies seem to indicate that’s not as much of a concern, except possibly in two cases: one, when the ratio of fructose to glucose consumption is high, or in cases of high consumption of calories. I would say that we have a combination of those, a relatively high ratio of fructose to glucose consumption (look at the relative amounts of HFCS to refined sugars used by beverage manufacturers!) together with consuming too many calories from sugar. (And remember, that’s just the average amount. Some people are consuming even larger amounts of sugar.)

Background on high fructose syrups

I recently came across a very interesting article, coauthored by John S. White, who is, or at least has been, a consultant to the Corn Refiners Association.

The article describes the manufacturing and refining process of HFCS (or, as the authors call it, HFS), the composition of various grades of HFCS (as well as crystalline fructose and crystalline fructose syrup), functional properties and uses, and regulatory status.

What I found so fascinating about this particular article though, were these bits of information scattered throughout it. According to the authors , HFS-42 (that is, HFCS that is 42% fructose) was the “first generation syrup of commerce.” (p.726S)

They go on to note that :

Japanese and US manufacturers were producing HFS containing 55% fructose by the late 1970s. HFS-55 was adopted by the carbonated-beverage industry and became the predominant sweetener in colas by late 1984. (p.726S)

On p. 727S, a table showing the typical composition of the various grades of fructose (ranging from 42% all the way up to 80% and 95%).

One of the minor differences between HFS-80 and HFS-95 is that they, unlike the other two, contain less sulfated ash and no sulfur dioxide. (Okay, the HFS-42 and -55 contain only 2 parts per million.)

The crystalline fructose and crystalline fructose syrup are both 99.5% or greater fructose.

What is interesting is that the authors note, p. 731S, that HFS-55 was being used in colas by late 1984, but that in 1988 the FDA had “proposed to recognize the long history of safety for fructose and reaffirm the GRAS status of HFS as a direct human food ingredient.” (FDA, 1992, 21 CFR 182.1866) GRAS = “Generally Recognized As Safe” (for particular uses of a substance), CFR = Code of Federal Regulations

They go on to note: “The petition is specific for HFS-42, but may include HFS-55 on review of its additional processing steps.”

I’m not a lawyer, but to me that sounds like HFS-55 had not actually been approved for use as a direct human food ingredient at the time that cola manufacturers were starting to use it. (I guess they must have just done that after the fact.)

HFS-55 vs. HFS-42

“The carbonated beverage industry is the largest user of HFS-42 and -55.” (p. 729S) HFS-42 is primarily used in non-colas and HFS-55 in many colas, though colas can also be made using more HFS-42. (See the graphic above about the use of sugar vs. HFCS by food vs. beverage manufacturers.)

In 1993 more than than 90% of energy-containing carbonated beverages produced in the U.S. were sweetened with HFS.

If I understand Hannover and White correctly, before 1984 most colas apparently were sweetened with HFS-42 and after 1984 with HFS-55. In other words, the HFCS had approximately a 13% increase in the amount of fructose in it after the switch.

More importantly, the ratio of fructose to glucose changed from 42:53 to 55:42. Why is that important?

Fructose malabsorption

Too much fructose in the diet can cause irritable bowel syndrome and other gastrointestinal problems. However, studies have found that the problems are reduced when fructose is consumed with glucose. (A certain percentage of the population is more prone to this, but it doesn’t seem to be an issue for most people.)

This is where you run into the problems of fructose metabolic products related to metabolic syndrome. (The results of some studies also suggested that fructose malabsorption and metabolism problems were more likely to be associated with copper deficiency.)

Is HFCS the biggest problem?

I was going to say that HFCS is not the innocent player some portray it to be, then I realized that’s not really accurate. The use of HFCS is not in and of itself the problem; the problem is food and beverage manufacturers putting it in almost every food and beverage they can. It’s cheaper than refined sugar. And most fast food places and restaurants reportedly make a higher profit margin off of soft drinks. Once HFCS was introduced soft drink ingredients became so inexpensive that a lot of places started offering free refills. I’m sure someone has brought that up before, but perhaps free refills are one of the main contributing factors to the increase in obesity (!?). When people had to pay for a second glass of soda, they drank less. Sorry, I don’t have a citation for that, but that seems obvious. (Okay, I had to check. I did a search on Google Scholar on +”obesity epidemic” +”free refills” and got 21 hits. Google Scholar searches the scientific literature and books, as opposed to the entire Web.)

Put that together with chronic overconsumption of sugar (regardless of whether they’re fructose or sucrose), unbalanced diets (deficiencies in vitamin D?), and not as much exercise as we should be getting.

Then throw in genetics, add a good dose of epigenetics in the form of gene-environment interactions, and you have all the conditions for development of metabolic syndrome and an obesity epidemic.

I personally am very interested in this topic because just over three years ago I had gone in to see my doctor because of abdominal pain. My triglycerides and LDL were high. He thought it might be my gallbladder so I went in for an ultrasound, which revealed that I had a fatty liver.

Fatty liver disease has not been considered a children’s disease, so it’s disturbing to read that children and adolescents are developing it, especially since there are usually few symptoms until the disease has progressed to a more advanced stage of steatohepatitis (aka hepatosteatosis) and scarring has already occurred.

According to the American Heart Association, more than 6 million children in the United States are affected.

The overweight children with NAFLD had significant cardiovascular risk including higher levels of fasting glucose, insulin, total cholesterol, low-density lipoprotein (LDL, “bad” cholesterol), triglycerides and higher systolic and diastolic blood pressure than the control group.

NAFLD is the most common cause of liver disease in children and is associated with metabolic syndrome, a clustering of risk factors for the development of cardiovascular disease and type 2 diabetes. NAFLD is characterized by the presence of oily droplets of triglycerides in liver cells. More than 6 million children in the United States are affected.

NAFLD in overweight children is strongly associated with metabolic syndrome. The association is independent of both body mass index and insulin sensitivity.

Fatty liver disease often has no outward symptoms, which contributes to it going undetected. Although some children will have symptoms such as abdominal pain or fatigue, the majority remain symptom-free until the disease is in very advanced stages.

Since 2003, substantial new informationhas emerged in children on the clustering of obesity, insulinresistance, inflammation, and other risk factors and their collectiverole in conveying heightened risk for cardiovasculardisease and type 2 diabetes. A constellationof these interrelated cardiovascular risk factors in adultshas come to be known as the metabolic syndrome.

Risk Factors for Metabolic Syndrome
The AHA lists heredity, ethnic differences, and lifestyle behaviors such as TV watching behavior, physical activity, and dietary intake, but does not discuss the possible role of other environmental factors)

Steinberger J, Daniels SR. Obesity, insulin resistance, diabetes and cardiovascular risk in children: an American Heart Association scientific statement from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Circulation. 2003; 107: 1448–1453.[Free Full Text]

Non-alcoholic fatty liver disease (NAFLD)

Once considered an illness of adults over 40, more and more children are being diagnosed with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). NAFLD can be a precursor to NASH, which can progress to cirrhosis.

When complications such as cirrhosis cannot be controlled with treatment or when the liver becomes so damaged from scarring that it completely stops functioning, a liver transplant is necessary.

Both NASH and NAFLD are becoming more common, possibly because of the greater number of Americans with obesity. In the past 10 years, the rate of obesity has doubled in adults and tripled in children. Obesity also contributes to diabetes and high blood cholesterol, which can further complicate the health of someone with NASH. (From the NASH page on the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) website.)

In case you’re wondering what I did after my diagnosis…

At the ultrasound the technician had said, “Your gallbladder is fine, but you have a fatty liver.” The way she said it made it sound like it was more than just a casual observation, so when I got home I did a quick search on the National Library of Medicine’s website, where I found a lot of information about NAFLD. (I’m not a teetotaler, but I don’t drink much.)

The progression from NAFLD to NASH to cirrhosis to needing a liver transplant or you die got my attention. Even before I got the formal diagnosis from my doctor I changed my diet (I started eating fish, raisins, and nuts, as well as more fruit, nuts, raisins, whole grains, leafy green vegetables, and fiber (even tried quinoa); and fewer sugar-sweetened drinks) and lots more exercise. I dropped about twenty pounds in four months and, more importantly, my triglyceride level dropped a lot.

I had relapsed a bit since then, but after viewing Dr. Lustig’s presentation on the effects of fructose (and having done some follow up reading on the topic) I have once again cut back on sugar consumption and have started working out more regularly once more.

Take a spoonful of sugar, add a pinch of chemicals that accumulate in fatty tissue, and voila, metabolic syndrome! So while Dr. Lustig may be on to something, it looks like fructose might not be the only thing to blame for the obesity epidemic.

The reason why persistent organic pollutants (POPs) are a problem is that they can bioaccumulate in fatty tissue. (If fructose causes metabolic syndrome as Dr. Lustig says, and metabolic syndrome results in increased obesity, which in turn means more fatty tissue, and more fatty tissue can absorb more POPs, we would seem to have started a rather vicious cycle.)

The Editor’s Summary explains why the findings of this study are especially important (emphasis added).

The authors conclude that exposure to POPs through a diet high in fatty fish is capable of inducing insulin resistance and impairing both lipid and glucose metabolism. Furthermore, they found that n-3 polyunsaturated fatty acids failed to counteract the harmful metabolic effects of dietary POP exposure. This finding is important because the presence of n-3-polyunsaturated fatty acids in fish oil has been reported to have a wide range of beneficial effects, including protection against high-fat diet–induced insulin resistance. The authors conclude that there is a need to continue efforts to limit human exposure to dietary POPs even in foods containing protective factors such as polyunsaturated fatty acids.

On Feb. 9, 2010, President Obama created the first-ever federal task force to enhance coordination between private sector companies, not-for-profits, agencies within the government and other organizations to address the problem of childhood obesity. The Presidential Memo that established the Task Force directed senior officials from executive agencies and the White House to develop a comprehensive interagency action plan that details a coordinated strategy, identifies key benchmarks and goals, describes research gaps and needs, and assists in the development of legislative, budgetary, and policy proposals that can improve the health and well-being of children, their families, and communities.

Now, Dr. Robert Lustig spoke about the basic problem with FDA and USDA on this issue in a lecture (see “The toxic effects of … sugar“). He said that the biggest problem is not lack of exercise, but ingesting too much fructose. (If lack of exercise is the reason, explain why there’s an epidemic of obese six-month-olds.)

Lustig says that the studies linking fat consumption and heart disease did not control for sugar consumption. He pointed out that in Western societies high-fat diets are high-sugar diets. And he said that FDA won’t regulate fructose because it’s not an acute toxin, but a chronic toxin leading to metabolic syndrome (plus, the FDA considers it “natural”—which Dr. Lustig notes is true only on the technicality that HFCS is made from a natural product—HFCS is highly processed and refined). And the USDA, which controls the food pyramid, won’t touch high fructose corn syrup because it’s made from corn. (See also “Junk food turns rats into addicts. Bacon, cheesecake, Ho Hos alter brain’s pleasures centers.”)

The Federal Register notice points people to First Lady Michelle Obama’s “Let’s Move” initiative – http://www.letsmove.gov/. I certainly support this, but I think they need to go further and start looking at the connection between fructose and obesity. The site has links to all sorts of useful information, including a link to the Food Environment Atlas from USDA which shows consumption of various foods around the U.S., as well as maps showing diabetes and obesity rates (under “Health”).

While there’s no acknowledgement that the type of sugar we’re consuming has an effect, I did notice that there are signs that someone in the government is paying attention. Water is recommended as the main drink. Fruit juices are discouraged, as are “added sugars.” But they don’t appear to have made the leap yet to the connection between fructose and the metabolic syndrome, which appears to be even more important than the number of calories consumed or burned.